The myocardial β-adrenergic system in spontaneously hypertensive heart failure (SHHF) rats
The myocardial β-adrenergic system in spontaneously hypertensive heart failure (SHHF) rats
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DOI：
10.1161/01.hyp.33.1.402
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发表时间：
1999-01-01
期刊：
影响因子：
8.3
通讯作者：
Koch, WJ
中科院分区：
文献类型：
--
作者：
Anderson, KM;Eckhart, AD;Koch, WJ
在衰竭的人类心肌中，对β-肾上腺素能刺激的反应性降低。这主要是由于β-肾上腺素能受体（β AR）密度降低、β-肾上腺素能受体激酶1（β ARK 1）水平升高以及其余受体的功能性解偶联所致。人类心肌β-肾上腺素能系统相对于症状性心力衰竭（HF）发作的变化的时间性质一直难以辨别。一种相对较新的HF模型，自发性高血压心力衰竭（SHHF）大鼠自发地和可重复地发展左心室肥大（LVH）并进展为HF，从而使纵向研究能够检查高血压诱导的心脏肥大和随后的HF的细胞和分子基础。本研究的目的是检查该模型中β AR系统的年龄依赖性变化。将3、7、14和20个月时的瘦型雄性SHHF大鼠与年龄匹配的Sprague-Dawley（SD）对照大鼠进行比较（[C]; 4只动物/组）。与SD对照组相比，SHHF组各年龄组大鼠血压和左室舒张末期压均升高（P
Responsiveness to beta-adrenergic stimulation is reduced in the failing human myocardium. This results principally from reduced beta-adrenergic receptor (beta AR) density, elevated beta-adrenergic receptor kinase 1 (beta ARK1) levels, and functional uncoupling of remaining receptors, The temporal nature of changes in the human myocardial beta-adrenergic system relative to onset of symptomatic heart failure (HF) has been difficult to discern. A relatively new model of HF, the spontaneously hypertensive heart failure (SHHF) rat spontaneously and reproducibly develops left ventricular hypertrophy (LVH) and progresses to HF, thus enabling longitudinal studies to examine the cellular and molecular bases for hypertension-induced cardiac hypertrophy and subsequent HF. The purpose of this study was to examine age-dependent changes in the beta AR system in this model. Lean male SHHF rats at 3, 7, 14, and 20 months were compared with age-matched Sprague-Dawley (SD) control rats ([C]; 4 animals/group). At all ages the SHHF rats had elevated blood pressures and left ventricular end-diastolic pressure relative to the SD control rats (P